Cartilage homeostasis in health and rheumatic diseases
By M. Goldring, K. Marcu. Arthritis Research & Therapy, 2009
757 citations recorded by the source corpus.
As the cellular component of articular cartilage, chondrocytes are responsible for maintaining in a low-turnover state the unique composition and organization of the matrix that was determined during embryonic and postnatal development. In joint diseases, cartilage homeostasis is disrupted by mechanisms that are driven by combinations of biological mediators that vary according to the disease process, including contributions from other joint tissues. In osteoarthritis (OA), biomechanical stimuli predominate with up-regulation of both catabolic and anabolic cytokines and recapitulation of developmental phenotypes, whereas in rheumatoid arthritis (RA), inflammation and catabolism drive cartilage loss. In vitro studies in chondrocytes have elucidated signaling pathways and transcription factors that orchestrate specific functions that promote cartilage damage in both OA and RA. Thus, understanding how the adult articular chondrocyte functions within its unique environment will aid in the development of rational strategies to protect cartilage from damage resulting from joint disease. This review will cover current knowledge about the specific cellular and biochemical mechanisms that regulate cartilage homeostasis and pathology.
Subfields: Pharmacology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/d62e672a25b293a4d2ab0a68fd5c6720cf00f098
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In Pharmacology
In Rheumatology
Citations in the corpus
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets (2023, background): “These transcription factors trigger the expression of ADAMTS5 and MMP13 proteases, which promotes the differentiation of pre-hypertrophic articular chondrocytes to terminal differentiated chondrocytes.(199) In addition, Deng and coworkers found that inflammatory cytokines regulated TAK1-mediate-phos”
- Osteoarthritis: a disease of the joint as an organ. (2012, background): “The most extensively studied are IL-1β and TNFα, which can suppress matrix synthesis and promote cartilage catabolism (6).”